ABT-510 acetate (1, 5, 10, 20, 50 nM; 24 h) induces apoptosis in ID8 cells and increases the incidence of apoptosis in the human epithelial cancer cell lines SKOV3, OVCAR3, and CAOV3[1].
ABT-510 acetate (0-10 μM; 7 days) inhibits NO-stimulated vascular cell outgrowth into and invasion through extracellular matrix. ABT-510 acetate blocks tumor-driven vascular cell outgrowth, NO-driven cGMP flux, and CD36-mediated fatty acid uptake. [3].
ABT-510 acetate (100 mg/kg; i.p.; single daily for 90 days) induces cells apoptosis in vivo and leads to a significant reduction in epithelial ovarian tumor size, ascites fluid volume, and secondary lesion dissemination in mice[1].
ABT-510 acetate (60 mg/kg; osmotic minipumps for s.c.; single daily for 7 days) decreases angiogenesis and inflammation in a murine model of inflammatory bowel disease[2].
References:
[1]. Greenaway J, et.al. ABT-510 induces tumor cell apoptosis and inhibits ovarian tumor growth in an orthotopic, syngeneic model of epithelial ovarian cancer. Mol Cancer Ther. 2009 Jan;8(1):64-74.
[2]. Punekar S,et.al. Thrombospondin 1 and its mimetic peptide ABT-510 decrease angiogenesis and inflammation in a murine model of inflammatory bowel disease. Pathobiology. 2008;75(1):9-21.
[3]. Isenberg JS, et.al. Differential effects of ABT-510 and a CD36-binding peptide derived from the type 1 repeats of thrombospondin-1 on fatty acid uptake, nitric oxide signaling, and caspase activation in vascular cells. Biochem Pharmacol. 2008 Feb 15;75(4):875-82.